The Effects Of Glucagon-like Peptide-1 On Injury Of Cultured Cardiomyocytes Induced By Hypoxia/reoxygenation

Objective:1. To culture neonate rat cardiomyocytes in vitro.2. To study the effect of glucagon-like peptide-1(GLP-1) oncardiomyocytes injury induced by hypoxia/reoxygenation(H/R) to verifyweather GLP-1 could protect the heart.3. To supply theory foundation for the security and validity of GLP-1and correlated drug in clinical application.Method:1. The cultured neonate rat cardiomyocytes were characterized bymicroscope observation and immunohistochemistry method.2. Primary cultured cardiomyocytes were randomly divided into threegroups: normal control group (group A), H/R group (hypoxia for 16 hours,reoxygenation for 4 hours, group B), H/R and GLP-1 group (group C).3. The activity of lactate dehydrogenase in the culture medium wasdetected by test kit.4. Stained with propidium iodide, cardiomyocytes apoptosis rate wasdetected by flow cytometry.5. Caspase-3 activity was detected by test kit.Result:1. Cardiomyocytes were confirmed and these purity was more than 90％.2. Activity of LDH: Compared with group A, the activity of LDH increasedsignificantly in group B(210.0±11.5 U/L vs 101.4±6.5U/L,P＜0.01).Compared with group B, the activity of LDH decreased in group C(190.2±9.0 U/L vs 210.0±11.5 U/L, P＜0.01).The differences between them all have statistical significance.3. Cardiomyocytes apoptosis rate: Compared with group A, apoptosis rateincreased significantly in group B(8.138±1.512 vs0.575±0.167,P＜0.01). Compared with group B, apoptosis rate decreased significantlyin groupC (2.688±0.589 vs 8. 138±1.512, P＜0.01).The differences betweenthem all have statistical significance.4. Caspase-3 activity: Compared with group A, caspase-3 activityincreased significantly in group B(445155.1±56914.2 vs 199813.1±19695.5, P＜0.01).Compared with group B, caspase-3 activity decreasedsignificantly in group C(445155.1±56914.2 vs 303394.3±41757.8, P＜0.01). The differences between them all have statisticalsignificance.Conclusion:It was demonstrated in our vitro study that GLP-1 can directly acton cardiomyocytes and protect them from H/R injury mainly by inhibitingtheir apoptosis, the mechanism of which may be concerned with GLP-1's effects on apoptotic or antiapoptotic pathways including caspase-3.